In a typical migraine, a throbbing headache quickly follows the visual symptoms. The headache lasts several hours and is accompanied by nausea and sensitivity to light and sound. The intensity of the headache may range from mild to severe.
An isolated visual migraine, without headache, typically does not require any acute treatment, since the visual symptoms resolve on their own fairly quickly. The first few times someone experiences a visual migraine it usually causes a lot of anxiety. Once someone has become familiar with the symptoms of a visual migraine, new episodes no longer cause the same level of anxiety.
Background: The American Headache Society previously published a Consensus Statement on the use of newly introduced treatments for adults with migraine. This update, which is based on the expanded evidence base and emerging expert consensus concerning postapproval usage, provides practical recommendations in the absence of a formal guideline.
We conducted the largest GWAS meta-analysis on migraine thus far by combining genetic data on 102,084 cases and 771,257 controls. We identified 123 migraine risk loci, of which 86 are previously unknown since the previous migraine meta-analysis, which yielded 38 loci13. This shows that we have now reached the statistical power for rapid accumulation of new risk loci for migraine, in line with the progress of GWAS seen with other common diseases54, and as expected for a highly polygenic disorder like migraine55.
With respect to a vascular involvement in the pathophysiology of migraine, both gene expression and chromatin annotation data from LDSC-SEG showed that migraine signals are enriched for genes and cell-type-specific annotations that are highly expressed in aorta and tibial and coronary arteries. The involvement of arteries was also proposed by our DEPICT tissue enrichment analysis. In addition, cardiovascular disease and blood pressure phenotypes were among the top categories in the PheWAS analyses. These results are consistent with previous reports of a shared etiology and some genetic correlation between migraine and cardiovascular and cerebrovascular endpoints47,48,49,63,64,65,66,67. However, in our analysis, the migraine risk alleles neither consistently increased nor consistently decreased the risk of CAD or the risk of hypertension.
A key role of the CNS in migraine pathophysiology has emerged from animal models, human imaging and neurophysiological studies10,68, while support for CNS involvement from genetic studies has been more difficult to obtain. A likely reason is the paucity of gene expression data from CNS tissue types, but recently more data have become available, making such studies feasible. Our LDSC-SEG analysis using gene expression data from 13 brain regions showed an enrichment for caudate nucleus in the basal ganglia, and with chromatin-based annotations for five CNS tissue types: dorsolateral prefrontal cortex, neurospheres derived from cortex, fetal brain, germinal matrix and neurospheres derived from ganglion eminence. Alterations in the structure and/or function of several brain regions68,69,70, including basal ganglia, cortex, hypothalamus, thalamus, brainstem, amygdala and cerebellum, have been reported for individuals who suffer from migraine, but the cause of these changes is not known.
Even though we observed links between our new risk loci and known target genes of effective migraine drugs, the accurate gene prioritization at risk loci remains challenging. First, robust fine-mapping would require accurate LD information79, which is typically lacking in meta-analyses and further distorted from reference panels by variation in effective sample size across variants. Second, computational approaches to gene prioritization require further methodological work80 and extension to additional sources of functional data to provide more robust and comprehensive gene prioritization results. Another limitation of our study is that a large proportion of migraine diagnoses are self-reported. Therefore, we cannot rule out misdiagnosis, such as, for example, tension headache being reported as migraine, which could overemphasize genetic factors related to general pain mechanisms and not migraine per se. Regardless, the high genetic correlation that we observed supports a strong phenotypic concordance between the study collections that also included deeply phenotyped clinical cohorts from headache specialist centers, which were instrumental for the migraine subtype analyses. While the subtype data provided convincing evidence of both loci with genetic differences and other loci with genetic overlap between subtypes, larger samples are still needed to achieve a more accurate picture of the similarities and differences in genetic architecture behind the subtypes.
If you have migraine, your GP or nurse can give advice on reducing your risk of a stroke from any other health conditions you may have, like high blood pressure, diabetes, atrial fibrillation or high cholesterol. They can also support you with making lifestyle changes such as stopping smoking, losing weight, healthy eating and exercise.
Migraine affects around one in every 15 men, and one in five women. People of all ages are affected by migraine, but the condition often begins in young adulthood. It often runs in families, and many people with migraine have a close relative with the condition. Some people have several migraines a week; others may have years between migraine attacks. Symptoms can last from a few hours to several days, and you may also feel very tired for up to a week after an attack. Migraine without aura
Some people are able to avoid their triggers and so eliminate migraine that way. Many people find that ordinary painkillers such as paracetamol, ibuprofen and aspirin reduce the pain of their migraine headache. Do not take painkillers every day for a migraine, as painkiller over-use can cause headaches. Your GP or a specialist can prescribe other treatments for nausea.There are medications you can take at the start of an attack to stop it developing, and others that you take regularly to make attacks less frequent or less intense (prophylactic medication). Botulinum toxin type A treatment (often known as Botox) is available for some cases of chronic migraine.
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